Prostate cancer cells respond to irradiation by increasing SIRT1 expression (Fig. 2) to transiently increase glycolysis, by stabilizing p53 (Fig. 3), and mitochondrial biogenesis, by potentiating PGC-1α activity (Fig. 4), to sustain immediate and long-term energy requirements (Fig. 5) [20, 34]. The gene discussed is TP53; the disease is prostate carcinoma.